Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Src kinases involved in hepatitis B virus replication.

N P Klein1, M J Bouchard, L H Wang

  • 1Department of Microbiology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.

The EMBO Journal
|September 16, 1999
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[Glioblastoma with loss of H3K27me3 and EGFR exon 20 insertion: report of a case].

Zhonghua bing li xue za zhi = Chinese journal of pathology·2026
Same author

[Analysis of influencing factors of incisional infection and construction of risk prediction model in laparoscopic colorectal cancer surgery].

Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery·2026
Same author

[Value of quantitative p53 IHC in predicting TP53 mutation status: a study in lung adenocarcinoma].

Zhonghua bing li xue za zhi = Chinese journal of pathology·2026
Same author

Enhanced S-Factor for the ^{14}N(p,γ)^{15}O Reaction and Its Impact on the Solar Composition Problem.

Physical review letters·2025
Same author

[Expert consensus on the clinical application of endometrial ablation].

Zhonghua fu chan ke za zhi·2025
Same author

[Comparison between the Six Modes of Depression and the theory of Rufus in his <i>On Melancholy</i>].

Zhonghua yi shi za zhi (Beijing, China : 1980)·2025
Same journal

Scalable phosphotyrosine enrichment with SH2 superbinder enables deep profiling of EGF responses.

The EMBO journal·2026
Same journal

Essential nucleus-apical pole linkage maintains division fidelity during Plasmodium progeny formation.

The EMBO journal·2026
Same journal

From cell atlases to mechanisms: bridging scRNA-seq discovery with in vivo genetics.

The EMBO journal·2026
Same journal

Mitochondrial calcium regulates lipid metabolism by modulating tethering of mitochondria to lipid droplets.

The EMBO journal·2026
Same journal

Chromosome condensation mechanically primes the nucleus for mitosis.

The EMBO journal·2026
Same journal

NDR kinase SAX-1 controls dendrite branch-specific elimination during neuronal remodeling in C. elegans.

The EMBO journal·2026
See all related articles

Hepatitis B virus HBx protein activates Src tyrosine kinases, promoting viral replication and reverse transcription. Inhibiting Src kinase significantly impairs hepatitis B virus replication.

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Chronic hepatitis B virus (HBV) infection is a major cause of liver cancer and disease.
  • The HBV HBx protein is crucial for viral infection and implicated in liver disease pathogenesis.
  • HBx is known to modulate cellular signaling pathways, including Src tyrosine kinases and Ras-GTPases.

Purpose of the Study:

  • To investigate the role of HBx-mediated signaling in HBV replication.
  • To determine whether HBx activation of Src tyrosine kinases or Ras-GTPases is essential for viral replication.

Main Methods:

  • Utilized cell culture models of HBV infection.
  • Assessed viral replication and reverse transcription.
  • Employed targeted inhibition of Src tyrosine kinase activity and HBx gene manipulation.

Related Experiment Videos

  • Investigated the subcellular localization of HBx and its impact on signaling.

    • Main Results:

    • HBx activation of Src tyrosine kinases, but not Ras-GTPases, significantly promotes HBV replication in cell culture.
    • HBx stimulates the reverse transcription of viral pregenomic mRNA into genomic DNA via a Src-mediated pathway.
    • Inhibition of Src tyrosine kinase activity, HBx gene inactivation, or disruption of cytoplasmic HBx signaling strongly impaired viral reverse transcription.

    Conclusions:

    • HBx protein's stimulation of the Src family of tyrosine kinases is critical for enhancing HBV replication.
    • The Src-mediated pathway activated by HBx plays a key role in regulating viral polymerase activity and reverse transcription.